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Maj (Dr.) Jane Alam Mamun
Dept of Ortho Surgery,
Combined Military Hospital,
Dhaka, Bangladesh
GOUTY ARTHITIS
“The disease of the kings and the King of the Diseases”
What is Gout/Gouty Arthritis?
It is a crystal deposition disease caused by
deposition of monosodium urate crystals in joints
and other tissues, secondary to hyperuricaemia.
Synonym:
• Podagra
• Urate crystal synovitis
• The disease of Kings or Rich man’s disease
History
• 2640 BC: Podagra (from the Greek for ‘foot
trap’) first identified by the Egyptians.
• 5th Century BC: Hippocrates referred to gout
as “unwalkable disease.
• The term ‘gout’ derives from the Latin word
‘gutta’ meaning a ‘drop’.
• In 1683 : The English physician Thomas
Sydenham, himself a sufferer, gave a detailed
clinical description of gout.
The Disease of the ‘KINGS’
or
The Richman’s Disease
Rich foods have a higher concentration of
protein.
The Kings of Pain
• Benjamin Franklin
• Thomas Jefferson
• Sir Isaac Newton
• Charles Darwin
• King Henry VIII and many
other famous leaders also
suffered from gout
Epidemiology
• Most common inflammatory joint disease in
men with peak onset in the fifth decade.
• A second group are older females, invariably
on diuretics.
• Prevalence of gout is 1–2.5% of adults in
developed countries .
• Deficiency of hypoxanthine– guanine
phosphoribosyl transferase (HGPRT) is seen to
be associated.
Incidence
As per ACR:
Frequent Low Back Pain
40.2 million in 2005, projected to increase to 48.6
million in2025
Osteoarthritis
20.7 million in 2005, projected to increase to 28.1
million in 2025
Gout
2.6 million in 2005, projected to increase to 3.6 million
in 2025
Rheumatoid Arthritis
2.1 million in 2005, projected to increase to 2.8 million
in 2025
Predisposing factors
• Family history (30-40%)
• Alcohol abuse (50%)
• Purine rich foods – meat, kidney, liver, seafood,
anchovies, oatmeal, certain vegetables (peas,
beans, lentils, mushrooms, cauliflower, spinach),
sweetbreads, Caffeine
• Drugs – Loop diuretics, NSAIDs, corticosteroids,
Niacin, Sinemet, Cyclosporine, Salicylates,
Ethambutol, Pyrazinamide
• Trauma
• Infection
• Other comorbid diseases – DM, HTN, Obesity,
vascular dx, renal dx, thyroid dx, sarcoidosis, etc.
Uric Acid Metabolism
• Normal S. Uric acid level:
– 4.0 to 8.6 mg/dl (in men)
– 3.0 to 5.9 mg/dl (in women)
• Urinary levels are normal below 750 mg/ 24h.
Uric Acid Metabolism
Uric Acid Metabolism(Contd..)
Pathophysiology
• Sodium urate is deposited as
crystals on the surface of articular
cartilage.
• Then articular cartilage is eroded.
• The subchondral bone is replaced
by crystaline deposit (tophi).
• A pannus of granulation tissue
grows over the articular surface,
invades and replaces the cartilage .
• Then granulation tissue bridges the
joint to the opposite articular
surface and producing fibrous
ankylosis.
Microscopically
• The deposites are
surronded by
• an inflamatory
reaction,
• fibrous tissue and
• giant cells
Classification
Two major types:
1. Primary gout (95%)
2. Secondary gout (5%)
Four Stages Of Gouty Arthritis
This disorder can be progressive through
four stages if undertreated:
1. Asymptomatic Hyperuricemia
2. Acute Gout / Acute Gouty Arthritis
3. Interval / Intercritical
4. Chronic Tophaceous Gout
1. Asymptomatic hyperuricemia
• Serum [urate] abnormally high without SSx
– Male >420μmol/L (7 mg/dL)
– Female >360μmol/L (6mg/dL)
• Not life threatening and readily treatable
• Routine prophylactic treatment is NOT
required
2. Acute Gout
• Acute gout is a painful condition
that typically affects only one or a
few joints
• Throbbing, crushing, or excruciating
pain over hours frequently
nocturnal
• Precipitated by local trauma,
unaccustomed exercise and alcohol
consumption
• Joint appears swollen, red, warm,
and tender. Fever may be there.
• Usually affects monoarticular joint
and lower extremities (Metatarso
Phalyngeal joint, ankle and knee).
– 1st MTP classic presentation
– May also cause bursitis, tendinitis.
Acute Gout (Contd..)
• The attack may go away in a few days (usually
5-7 days), but may return from time to time.
• Additional attacks often last longer.
• After a first gouty attack, half of the people will
have no symptoms, half of patients have
another attack.
• Mimic septic arthritis, cellulitis or
thromboplebitis
3. Interval/ Intercritical gout
• Asymptomatic period
between crises
• Duration varies, but
untreated patients may have
a second episode within two
years.
• Some patients evolve to
chronic polyarticular gout
without pain free
intercritical episodes.
4. Chronic Tophaceous Gout
• Polyarticular arthritis + tophi formation
• Articular tophaceous gout may results in destructive
arthropathy and secondary OA
• Tophaceous disease more like to occur in patients with:
– Serum urate level >540 μmol/L (>9mg/dL)
– Disease onset at younger age (≤40 years)
• Sites of tophi:
– Digits of hands and feet (most common)
– Pinna of ear (classic, less common)
– Bursa around elbows and knees
– Achilles tendon
Diagnosis
1977 ACR Criteria for Acute gout
The presence of characteristic urate crystals in
the joint fluid, or a tophus proved to contain
urate crystals by chemical means or polarized
light microscopy, or the presence of 6 of the
following 12 clinical, laboratory, and radiographic
phenomena:
1. More than one attack of acute arthritis
2. Maximum inflammation developed within 1 day
3. Monoarthritic attack
4. Redness observed over joints
1977 ACR Criteria for Acute gout
(Contd..)
5. First metatarsophalangeal joint painful or
swollen
6. Unilateral first metatarsophalangeal joint
attack
7. Unilateral tarsal joint attack
8. Tophus (proven or suspected)
9. Hyperuricemia
10. Asymmetric swelling within a joint on x
ray/exam
11. Subcortical cysts without erosions on x ray
12. Joint fluid culture negative for organisms
during attack
Investigations
• Serum Uric acid
• Plain radiographs (may be normal)
• Synovial fluid analyis (shows uric acid crystals)
• BUN (blood urea nitrogen),
• Serum Creatinine
• Synovial biopsy
• 24 hours Uric acid in urine
• Inv for Comorbid diseases
• Routine:
– CBC with ESR
– CRP etc.
Biochemical Tests For Gout
SYNOVIAL FLUID ANALYSIS
(Polarized Light Microscopy)
• The Gold standard
• Urate Crystals during
attacks
• Needle & rod shapes
• Strong negative
birefringence
Radiograph
• Acute gouty arthritis
: normal; soft tissue
swelling
• Chronic tophaceous
gout :
– tophi,
– erosive bone lesions
(punched out
lesions),
– pathognomonic in
foot and big toe
Few Radiographs
Differential Diagnosis
• Septic Arthritis
• Pseudogout: Chondrocalcinosis, CPPD
• Rheumatoid arthritis
• Osteoarthritis
Treatment
TREATMENT GOALS
1. Rapidly end acute flares.
2. Protect against future flares.
3. Reduce chance of crystal induced
inflammation.
4. Prevent disease progression.
5. Lower serum urate to deplete total body urate
pool.
6. Correct metabolic cause.
Drugs Used In Treatment
• NSAIDs
– Naproxen
– Indomethacin
– Etoricoxib
• Steroid/ Colchicine
• ULT :
– 1st Line: Allopurinol / Febuxostat / Pegloticase
– 2nd Line: Uricosuric agents
• Probenecid
• Lesinurad
• Sulphinpyrazone
• Benzbromarone
ULT
Acute Gout - Rx
• NSAIDs (unless CRI, CHF,
PUD, etc.)
• Corticosteroids (Intra-
articular if one joint,
systemic if multiple joints)
• Colchicine (adjust dose in
patients with renal
insufficiency)
• Indomethacin 50mg BD
• Naproxen 500mg BD
• Sulindac 200mg BD
• 20-30mg/day if systemic used
• Most beneficial in first 12-36 hours of an
attack
• 1 mg initially, then 0.5mg qhr tappering
upto 7 days
• Renal dosing:
– If Cr clearance < 50, reduce dose 50%.
– If Cr clearance < 10, contraindicated.
Acute Gout – Rx (Contd..)
• Reassurance
• Rest of the limb
• Ice compresion
• Splintage if required
Intercritical Gout - Rx
Education, Lifestyle / Diet modification,
Pharmacotherapy modification
ULT (Allopurinol) therapy if:
• Recurrent attacks despite diet change.
• Hx of nephrolithiasis
• Serum creatinine > 2.0 mg/dl
• Serum uric acid > 11.0 mg/dl
• 24 hr urine uric acid > 800mg/dL
• Tophi present
Uricosuric (Probenecid) if:
• Recurrent attacks and 24hr urine uric acid <
800mg/dL
Allopurinol toxicity?
Colchicine
(NHS Fife, Gout Management Guidelines, 2010)
SURGERY
• May be req upto 5% of patients with gout due
to:
– Infection
– Poor hand function
– Intolerable deformity
Prevention
• Avoid purine rich foods –meats & vegetables like
spinach or mushrooms
• Reducing alcohol consumption
• Drinking adequate of Water.
• Weight reduction with proper diet and exercise
• Low-fat dairy foods may lower uric acid levels and
help manage gout.
• Avoid drinks high in sugar or fructose, like
concentrated juices or sodas.
• Avoid Diuretic Drugs.
Take Home Message
• Gout is often poorly diagnosed, so clinical
experience along with proper history taking is
essential to dx.
• Dietery modification, weight loss, and regular
exercise help manage gout and reduce flare risk.
• Patient Education & explanation is important.
• Gout & its Rx are often associated with high
blood pressure, and heart and kidney disease,
optimization of such comorbidities results in
better outcome.
Gouty Arthritis

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Gouty Arthritis

  • 1. Maj (Dr.) Jane Alam Mamun Dept of Ortho Surgery, Combined Military Hospital, Dhaka, Bangladesh
  • 2. GOUTY ARTHITIS “The disease of the kings and the King of the Diseases”
  • 3. What is Gout/Gouty Arthritis? It is a crystal deposition disease caused by deposition of monosodium urate crystals in joints and other tissues, secondary to hyperuricaemia. Synonym: • Podagra • Urate crystal synovitis • The disease of Kings or Rich man’s disease
  • 4. History • 2640 BC: Podagra (from the Greek for ‘foot trap’) first identified by the Egyptians. • 5th Century BC: Hippocrates referred to gout as “unwalkable disease. • The term ‘gout’ derives from the Latin word ‘gutta’ meaning a ‘drop’. • In 1683 : The English physician Thomas Sydenham, himself a sufferer, gave a detailed clinical description of gout.
  • 5. The Disease of the ‘KINGS’ or The Richman’s Disease Rich foods have a higher concentration of protein.
  • 6. The Kings of Pain • Benjamin Franklin • Thomas Jefferson • Sir Isaac Newton • Charles Darwin • King Henry VIII and many other famous leaders also suffered from gout
  • 7. Epidemiology • Most common inflammatory joint disease in men with peak onset in the fifth decade. • A second group are older females, invariably on diuretics. • Prevalence of gout is 1–2.5% of adults in developed countries . • Deficiency of hypoxanthine– guanine phosphoribosyl transferase (HGPRT) is seen to be associated.
  • 8. Incidence As per ACR: Frequent Low Back Pain 40.2 million in 2005, projected to increase to 48.6 million in2025 Osteoarthritis 20.7 million in 2005, projected to increase to 28.1 million in 2025 Gout 2.6 million in 2005, projected to increase to 3.6 million in 2025 Rheumatoid Arthritis 2.1 million in 2005, projected to increase to 2.8 million in 2025
  • 9. Predisposing factors • Family history (30-40%) • Alcohol abuse (50%) • Purine rich foods – meat, kidney, liver, seafood, anchovies, oatmeal, certain vegetables (peas, beans, lentils, mushrooms, cauliflower, spinach), sweetbreads, Caffeine • Drugs – Loop diuretics, NSAIDs, corticosteroids, Niacin, Sinemet, Cyclosporine, Salicylates, Ethambutol, Pyrazinamide • Trauma • Infection • Other comorbid diseases – DM, HTN, Obesity, vascular dx, renal dx, thyroid dx, sarcoidosis, etc.
  • 10. Uric Acid Metabolism • Normal S. Uric acid level: – 4.0 to 8.6 mg/dl (in men) – 3.0 to 5.9 mg/dl (in women) • Urinary levels are normal below 750 mg/ 24h.
  • 13. Pathophysiology • Sodium urate is deposited as crystals on the surface of articular cartilage. • Then articular cartilage is eroded. • The subchondral bone is replaced by crystaline deposit (tophi). • A pannus of granulation tissue grows over the articular surface, invades and replaces the cartilage . • Then granulation tissue bridges the joint to the opposite articular surface and producing fibrous ankylosis.
  • 14. Microscopically • The deposites are surronded by • an inflamatory reaction, • fibrous tissue and • giant cells
  • 15. Classification Two major types: 1. Primary gout (95%) 2. Secondary gout (5%)
  • 16. Four Stages Of Gouty Arthritis This disorder can be progressive through four stages if undertreated: 1. Asymptomatic Hyperuricemia 2. Acute Gout / Acute Gouty Arthritis 3. Interval / Intercritical 4. Chronic Tophaceous Gout
  • 17. 1. Asymptomatic hyperuricemia • Serum [urate] abnormally high without SSx – Male >420μmol/L (7 mg/dL) – Female >360μmol/L (6mg/dL) • Not life threatening and readily treatable • Routine prophylactic treatment is NOT required
  • 18. 2. Acute Gout • Acute gout is a painful condition that typically affects only one or a few joints • Throbbing, crushing, or excruciating pain over hours frequently nocturnal • Precipitated by local trauma, unaccustomed exercise and alcohol consumption • Joint appears swollen, red, warm, and tender. Fever may be there. • Usually affects monoarticular joint and lower extremities (Metatarso Phalyngeal joint, ankle and knee). – 1st MTP classic presentation – May also cause bursitis, tendinitis.
  • 19.
  • 20. Acute Gout (Contd..) • The attack may go away in a few days (usually 5-7 days), but may return from time to time. • Additional attacks often last longer. • After a first gouty attack, half of the people will have no symptoms, half of patients have another attack. • Mimic septic arthritis, cellulitis or thromboplebitis
  • 21.
  • 22. 3. Interval/ Intercritical gout • Asymptomatic period between crises • Duration varies, but untreated patients may have a second episode within two years. • Some patients evolve to chronic polyarticular gout without pain free intercritical episodes.
  • 23. 4. Chronic Tophaceous Gout • Polyarticular arthritis + tophi formation • Articular tophaceous gout may results in destructive arthropathy and secondary OA • Tophaceous disease more like to occur in patients with: – Serum urate level >540 μmol/L (>9mg/dL) – Disease onset at younger age (≤40 years) • Sites of tophi: – Digits of hands and feet (most common) – Pinna of ear (classic, less common) – Bursa around elbows and knees – Achilles tendon
  • 24.
  • 26. 1977 ACR Criteria for Acute gout The presence of characteristic urate crystals in the joint fluid, or a tophus proved to contain urate crystals by chemical means or polarized light microscopy, or the presence of 6 of the following 12 clinical, laboratory, and radiographic phenomena: 1. More than one attack of acute arthritis 2. Maximum inflammation developed within 1 day 3. Monoarthritic attack 4. Redness observed over joints
  • 27. 1977 ACR Criteria for Acute gout (Contd..) 5. First metatarsophalangeal joint painful or swollen 6. Unilateral first metatarsophalangeal joint attack 7. Unilateral tarsal joint attack 8. Tophus (proven or suspected) 9. Hyperuricemia 10. Asymmetric swelling within a joint on x ray/exam 11. Subcortical cysts without erosions on x ray 12. Joint fluid culture negative for organisms during attack
  • 28. Investigations • Serum Uric acid • Plain radiographs (may be normal) • Synovial fluid analyis (shows uric acid crystals) • BUN (blood urea nitrogen), • Serum Creatinine • Synovial biopsy • 24 hours Uric acid in urine • Inv for Comorbid diseases • Routine: – CBC with ESR – CRP etc.
  • 30. SYNOVIAL FLUID ANALYSIS (Polarized Light Microscopy) • The Gold standard • Urate Crystals during attacks • Needle & rod shapes • Strong negative birefringence
  • 31. Radiograph • Acute gouty arthritis : normal; soft tissue swelling • Chronic tophaceous gout : – tophi, – erosive bone lesions (punched out lesions), – pathognomonic in foot and big toe
  • 33. Differential Diagnosis • Septic Arthritis • Pseudogout: Chondrocalcinosis, CPPD • Rheumatoid arthritis • Osteoarthritis
  • 35. TREATMENT GOALS 1. Rapidly end acute flares. 2. Protect against future flares. 3. Reduce chance of crystal induced inflammation. 4. Prevent disease progression. 5. Lower serum urate to deplete total body urate pool. 6. Correct metabolic cause.
  • 36. Drugs Used In Treatment • NSAIDs – Naproxen – Indomethacin – Etoricoxib • Steroid/ Colchicine • ULT : – 1st Line: Allopurinol / Febuxostat / Pegloticase – 2nd Line: Uricosuric agents • Probenecid • Lesinurad • Sulphinpyrazone • Benzbromarone
  • 37. ULT
  • 38. Acute Gout - Rx • NSAIDs (unless CRI, CHF, PUD, etc.) • Corticosteroids (Intra- articular if one joint, systemic if multiple joints) • Colchicine (adjust dose in patients with renal insufficiency) • Indomethacin 50mg BD • Naproxen 500mg BD • Sulindac 200mg BD • 20-30mg/day if systemic used • Most beneficial in first 12-36 hours of an attack • 1 mg initially, then 0.5mg qhr tappering upto 7 days • Renal dosing: – If Cr clearance < 50, reduce dose 50%. – If Cr clearance < 10, contraindicated.
  • 39. Acute Gout – Rx (Contd..) • Reassurance • Rest of the limb • Ice compresion • Splintage if required
  • 40. Intercritical Gout - Rx Education, Lifestyle / Diet modification, Pharmacotherapy modification ULT (Allopurinol) therapy if: • Recurrent attacks despite diet change. • Hx of nephrolithiasis • Serum creatinine > 2.0 mg/dl • Serum uric acid > 11.0 mg/dl • 24 hr urine uric acid > 800mg/dL • Tophi present Uricosuric (Probenecid) if: • Recurrent attacks and 24hr urine uric acid < 800mg/dL Allopurinol toxicity? Colchicine
  • 41. (NHS Fife, Gout Management Guidelines, 2010)
  • 42. SURGERY • May be req upto 5% of patients with gout due to: – Infection – Poor hand function – Intolerable deformity
  • 43. Prevention • Avoid purine rich foods –meats & vegetables like spinach or mushrooms • Reducing alcohol consumption • Drinking adequate of Water. • Weight reduction with proper diet and exercise • Low-fat dairy foods may lower uric acid levels and help manage gout. • Avoid drinks high in sugar or fructose, like concentrated juices or sodas. • Avoid Diuretic Drugs.
  • 44.
  • 45. Take Home Message • Gout is often poorly diagnosed, so clinical experience along with proper history taking is essential to dx. • Dietery modification, weight loss, and regular exercise help manage gout and reduce flare risk. • Patient Education & explanation is important. • Gout & its Rx are often associated with high blood pressure, and heart and kidney disease, optimization of such comorbidities results in better outcome.